title: [Influence of electroacupuncture on p38-mitogen activated protein kinase in substantia nigra cells of rats with Parkinson disease model].
abstract: OBJECTIVE
  To explore the role of inflammatory reaction mediated by p38-mitogen activated protein kinase (p38-MAPK) signal path on prevention and treatment of Parkinson disease (PD) model rats by electroacupuncture (EA).
  
  
  METHODS
  Thirty-two healthy male SD rats were randomly divided into a normal group, a sham operation group, a model group and an EA group, eight rats in each one. The PD model was established in the model group and EA group by subcutaneous injection of rotenone in skin-back area (2 mg/kg, dissolved in sunflower oil, 2 mg/mL in density), while the injection of sunflower oil emulsion without rotenone at the same point and quantity as the model group was applied in the sham operation group. The normal group was not given any intervention. The EA treatment (continuous wave, 2 Hz in frequency, 1 mA in intensity, 20 min) was applied at "Fengfu" (GV 16) and "Taichong" (LR 3) in the EA group, once a day for continuously 14 days. No treatment was given in the other groups. The expression of tyrosine hydroxylase (TH), phosphorylated p38-MAPK, cyclooxygenase-2 (COX-2) in the substantia nigra were detected with immunohistochemical method.
  
  
  RESULTS
  There was typical PD ethology change in the model group. Compared with the normal group and sham operation group, the expression of TH positive neuron in the substantia nigra in the model group was significantly decreased, while the expression of phosphorylated p38-MAPK and COX-2 were significantly increased (all P < 0.01). Compared with the model group, the expression of TH positive neuron in the EA group was apparently increased, while the expression of phosphorylated p38-MAPK and COX-2 were significantly decreased (all P < 0.01).
  
  
  CONCLUSIONS
  The EA therapy could obviously reduce the expression of inflammation mediator COX-2, inhibit the phosphorylation of p38-MAPK, reduce the damage of dopaminergic neurons in the rats with PD, and this effect may be related with the impact of p38-MAPK signal path
authors.affiliation: Orthopedics Department of Hubei University of CM, Wuhan 430065, China.
authors.forename: Shu-Ju
authors.initials: SJ
authors.lastname: Wang
authors.forename: Jian-Qiao
authors.initials: JQ
authors.lastname: Fang
authors.forename: Jun
authors.initials: J
authors.lastname: Ma
authors.forename: Yan-Chun
authors.initials: YC
authors.lastname: Wang
authors.forename: Xiao-Ling
authors.initials: XL
authors.lastname: Zeng
authors.forename: Dan
authors.initials: D
authors.lastname: Zhou
authors.forename: Guo-Jie
authors.initials: GJ
authors.lastname: Sun
mesh_terms: D000818:Animals; D051546:Cyclooxygenase 2 / Q000235:genetics / Q000378:metabolism; D015671:Electroacupuncture; D006801:Humans; D008297:Male; D010300:Parkinson Disease / Q000201:enzymology / Q000235:genetics / Q000628:therapy*; D010766:Phosphorylation; D051381:Rats; D017207:Rats, Sprague-Dawley; D013378:Substantia Nigra / Q000201:enzymology*; D014446:Tyrosine 3-Monooxygenase / Q000235:genetics / Q000378:metabolism; D048051:p38 Mitogen-Activated Protein Kinases / Q000235:genetics / Q000378:metabolism*
chemical_list: D014446:Tyrosine 3-Monooxygenase; D051546:Cyclooxygenase 2; D048051:p38 Mitogen-Activated Protein Kinases